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Journal articles on the topic 'Human lymphocyte'
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1
Schimpff, R. M., and A. M. Repellin. "In vitro effect of human growth hormone on lymphocyte transformation and lymphocyte growth factors secretion." Acta Endocrinologica 120, no. 6 (June 1989): 745–52. http://dx.doi.org/10.1530/acta.0.1200745.
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Abstract. Cultures of human blood peripheral lymphocytes were performed in the presence or absence of human growth hormone, and also of phytohemagglutinin and normal human serum 10%. After incubation for 48 h, the supernatants were tested for their ability to promote the uptake of [3H]thymidine into lectin-activated lymphocytes. Supernatants from lymphocyte-free control samples, treated in the same manner, were assayed under the same experimental conditions. Variance analysis of the different dose-response relationships was performed. The results of these in vitro experiments confirm that physiological levels of GH inhibit the lectin-induced lymphoproliferation and that lymphocytes secrete an 'activity' able to stimulate the incorporation of [3H]thymidine into lectin activated lymphocytes. Furthermore we show that: 1) Secretion of this lymphocyte-stimulating activity is increased by physiological levels of GH; 2) This lymphocytic secretion is not radioimmunoassayable IGF-I; 3) Using fast protein liquid chromatography (FPLC), this activity appears in fractions with various molecular weights.
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Jalkanen, ST, and EC Butcher. "In vitro analysis of the homing properties of human lymphocytes: developmental regulation of functional receptors for high endothelial venules." Blood 66, no. 3 (September 1, 1985): 577–82. http://dx.doi.org/10.1182/blood.v66.3.577.577.
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Abstract Circulating lymphocytes leave the blood by binding to specialized high endothelial cells lining postcapillary venules in lymphoid organs or sites of chronic inflammations, migrating through the vessel wall into the surrounding tissue. The capacity of lymphocytes to recognize and bind to high endothelial venules (HEVs) is thus central to the overall process of lymphocyte traffic and recirculation. We show that viable human lymphocytes bind selectively to HEVs in frozen sections of normal human lymph nodes, thus defining a simple in vitro model for the study of human lymphocyte homing properties. Optimal conditions for the quantitative analysis of lymphocyte-HEV interaction are described. Furthermore, by using this assay, we demonstrate that the ability of human lymphocyte populations to bind to HEVs parallels their presumed migratory status in vivo. Thus, thymocytes and bone marrow cells, which are sessile in vivo, bind poorly to HEVs in comparison with mature circulating lymphocytes in peripheral blood or in peripheral lymphoid tissues. These results indicate that HEV-binding ability is a regulated property of mature lymphocytes and, as demonstrated previously in animal models, probably plays a fundamental role in controlling lymphocyte traffic in humans. The in vitro model of lymphocyte-HEV interaction thus provides a unique means to assay the migratory properties of normal and neoplastic human lymphocyte subsets, to analyze the role of lymphocyte traffic mechanisms in normal and pathologic inflammatory reactions, and to define some of the molecular mechanisms responsible for the control of lymphocyte migration and positioning in humans.
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Jalkanen, ST, and EC Butcher. "In vitro analysis of the homing properties of human lymphocytes: developmental regulation of functional receptors for high endothelial venules." Blood 66, no. 3 (September 1, 1985): 577–82. http://dx.doi.org/10.1182/blood.v66.3.577.bloodjournal663577.
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Circulating lymphocytes leave the blood by binding to specialized high endothelial cells lining postcapillary venules in lymphoid organs or sites of chronic inflammations, migrating through the vessel wall into the surrounding tissue. The capacity of lymphocytes to recognize and bind to high endothelial venules (HEVs) is thus central to the overall process of lymphocyte traffic and recirculation. We show that viable human lymphocytes bind selectively to HEVs in frozen sections of normal human lymph nodes, thus defining a simple in vitro model for the study of human lymphocyte homing properties. Optimal conditions for the quantitative analysis of lymphocyte-HEV interaction are described. Furthermore, by using this assay, we demonstrate that the ability of human lymphocyte populations to bind to HEVs parallels their presumed migratory status in vivo. Thus, thymocytes and bone marrow cells, which are sessile in vivo, bind poorly to HEVs in comparison with mature circulating lymphocytes in peripheral blood or in peripheral lymphoid tissues. These results indicate that HEV-binding ability is a regulated property of mature lymphocytes and, as demonstrated previously in animal models, probably plays a fundamental role in controlling lymphocyte traffic in humans. The in vitro model of lymphocyte-HEV interaction thus provides a unique means to assay the migratory properties of normal and neoplastic human lymphocyte subsets, to analyze the role of lymphocyte traffic mechanisms in normal and pathologic inflammatory reactions, and to define some of the molecular mechanisms responsible for the control of lymphocyte migration and positioning in humans.
4
Landesberg, Regina, and Richard A. Insel. "Autologous mixed lymphocyte reaction in human neonatal lymphocytes." Human Immunology 24, no. 4 (April 1989): 231–38. http://dx.doi.org/10.1016/0198-8859(89)90017-7.
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Li, Lijin, Sharon M. Dial, Monika Schmelz, Margaret A. Rennels, and Neil M. Ampel. "Cellular Immune Suppressor Activity Resides in Lymphocyte Cell Clusters Adjacent to Granulomata in Human Coccidioidomycosis." Infection and Immunity 73, no. 7 (July 2005): 3923–28. http://dx.doi.org/10.1128/iai.73.7.3923-3928.2005.
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ABSTRACT The in situ immunologic response in human coccidioidomycosis remains undefined. To explore this further, pulmonary necrotizing coccidioidal granulomata were examined using immunohistochemical staining for lymphocyte subsets and for the cytokines interleukin-10 (IL-10) and gamma interferon (IFN-γ). Discrete perigranulomatous lymphocytic clusters were seen in eight of nine tissues examined. In these tissues, T lymphocytes (CD3+) significantly outnumbered B lymphocytes (CD20+) in the mantle area of the granulomata (P = 0.028), whereas the clusters were composed of roughly equal numbers of T and B lymphocytes. While the number of cells in the mantle expressing IL-10 was similar to those in the perigranulomatous clusters, there were significantly more cells expressing IFN-γ in the mantle than in the clusters (P = 0.037). Confocal microscopy revealed that CD4+ T lymphocytes and B lymphocytes are associated with IL-10 production. CD4+CD25+ T lymphocytes were identified in the perigranulomatous clusters but were not associated with IL-10 production. This is the first report noting perigranulomatous lymphocyte clusters and IL-10 in association with human coccidioidal granulomata and suggests that down-regulation of the cellular immune response is occurring within coccidioidal granulomata.
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Park, Suk W., Walter Royal, Richard D. Semba, Gordon W. Wiegand, and Diane E. Griffin. "Expression of Adhesion Molecules and CD28 on T Lymphocytes during Human Immunodeficiency Virus Infection." Clinical Diagnostic Laboratory Immunology 5, no. 4 (July 1, 1998): 583–87. http://dx.doi.org/10.1128/cdli.5.4.583-587.1998.
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ABSTRACT Adhesion molecules, which play a major role in lymphocyte circulation, have not been well characterized in human immunodeficiency virus (HIV) infection. T-lymphocyte populations, including CD3, CD4, CD28, and adhesion molecules (L selectin, LFA-1, VLA-4, and ICAM-1) were measured by flow cytometry in a cross-sectional study of 100 HIV-infected and 49 HIV-seronegative adults. HIV-infected adults had lower numbers of CD3+ lymphocytes expressing L selectin (P < 0.0001) and VLA-4 (P < 0.01) and higher numbers of CD3+ lymphocytes expressing LFA-1bright (P < 0.002) than did HIV-negative adults. By CD4+-lymphocyte count category (>500, 200 to 500, or <200 cells/μl), HIV-infected adults with more advanced disease had lower percentages of CD3+ lymphocytes expressing L selectin and VLA-4 and higher percentages of CD3+ lymphocytes expressing LFA-1. The percentages of CD3+ CD28+ lymphocytes and of CD3+L selectin+ lymphocytes were positively correlated (Spearman coefficient = 0.86; P < 0.0001), and the percentage of CD3+ CD28+ lymphocytes and the CD3+ LFA-1bright lymphocyte/CD3+LFA-1dim lymphocyte ratio were negatively correlated (Spearman coefficient = −0.92; P <0.00001). The results of this study suggest that HIV infection is associated with altered expression of adhesion molecules.
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Wu, N. W., S. Jalkanen, P. R. Streeter, and E. C. Butcher. "Evolutionary conservation of tissue-specific lymphocyte-endothelial cell recognition mechanisms involved in lymphocyte homing." Journal of Cell Biology 107, no. 5 (November 1, 1988): 1845–51. http://dx.doi.org/10.1083/jcb.107.5.1845.
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Tissue-specific interactions with specialized high endothelial venules (HEV) direct the homing of lymphocytes from the blood into peripheral lymph nodes, mucosal lymphoid organs, and tissue sites of chronic inflammation. These interactions have been demonstrated in all mammalian species examined and thus appear highly conserved. To assess the degree of evolutionary divergence in lymphocyte-HEV recognition mechanisms, we have studied the ability of lymphocytes to interact with HEV across species barriers. By using an in vitro assay of lymphocyte binding to HEV in frozen sections of lymphoid tissues, we confirm that mouse, guinea pig, and human lymphocytes bind to xenogeneic as well as homologous HEV. In addition, we show that mouse and human lymphoid cell lines that bind selectively to either peripheral lymph node or mucosal vessels (Peyer's patches, appendix) in homologous lymphoid tissues exhibit the same organ specificity in binding to xenogeneic HEV. Furthermore, monoclonal antibodies that recognize lymphocyte "homing receptors" and block homologous lymphocyte binding to peripheral lymph node or to mucosal HEV, also inhibit lymphocyte interactions with xenogeneic HEV in a tissue-specific fashion. Similarly, anti-HEV antibodies against organ-specific mouse high endothelial cell "addressins" involved in lymphocyte homing to peripheral lymph node or mucosal lymphoid organs, not only block the adhesion of mouse lymphocytes but also of human lymphocytes to target mouse HEV. The results illustrate a remarkable degree of functional conservation of elements mediating these cell-cell recognition events involved in organ-specific lymphocyte homing.
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Moriguchi, S., J. C. Jacksont, and R. R. Watson. "Effects of Retinoids on Human Lymphocyte Functions in vitro." Human Toxicology 4, no. 4 (July 1985): 365–78. http://dx.doi.org/10.1177/096032718500400402.
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1 E-Rosette formation in vitro, lymphocyte mitogenesis and natural killer (NK) activity of human blood lymphocytes were strongly inhibited by high concentration (10 -4 M) of retinol or retinal. Other retinoids at 10-4 M (retinoic acid and 13-cis-retinoic acid) and lower concentrations (10-7 or 10-9 M) of retinol, retinal and carotenes also inhibited E-rosette formation. 2 Lymphocyte transformation responses induced by concanavalin A (Con A) or pokeweed mitogen (PWM) were also inhibited while NK activity was not affected. 3 There was a remarkable depression of the total number of viable lymphocytes after incubation with retinol or retinal 10-4 M. However, other retinoids, 10-7 and 10-9 M of retinol and retinal and carotenes did not show marked decrease of lymphocyte number or viability even after prolonged incubation (48 h). 4 The mechanism of inhibition by retinol or retinal (10-4 M) is due in part to the decrease of viable lymphocytes. It is unclear how other retinoids, carotenes and lower concentrations (10-7 or 10-9 M) of retinol or retinal inhibit E-rosette formation or lymphocyte transformation.
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Sun, Anyuan, Haiming Wei, Rui Sun, Weihua Xiao, Yongguang Yang, and Zhigang Tian. "Human Interleukin-15 Improves Engraftment of Human T Cells in NOD-SCID Mice." Clinical and Vaccine Immunology 13, no. 2 (February 2006): 227–34. http://dx.doi.org/10.1128/cvi.13.2.227-234.2006.
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ABSTRACT Human nonobese diabetic-severe combined immune deficiency (NOD-SCID) mouse chimeras have been widely used as an in vivo model to assess human immune function. However, only a small fraction of transferred human T lymphocytes can be detected in human peripheral blood lymphocyte (huPBL)-NOD-SCID chimeras. To improve the reconstitution of human T lymphocytes in NOD-SCID mice, the use of recombinant human interleukin-15 (rhIL-15) as a stimulator of human lymphocytes was explored. Administration of rhIL-15 after transplantation of huPBLs into NOD-SCID mice increased reconstitution of human T lymphocytes in a dose-dependent manner, with an optimal dosage of 1 μg/mouse. The number of human T lymphocytes (HLA-ABC+ CD3+) in the lymphoid organs or tissue of rhIL-15-treated huPBL-NOD-SCID mice increased 11- to 80-fold, and phytohemagglutinin-induced T-lymphocyte proliferation and cytokine production were significantly enhanced. Additionally, although mature human cells have not been thought to enter the murine thymus, human T lymphocytes were detected in the huPBL-NOD-SCID thymus after rhIL-15 treatment. Thus, rhIL-15 can be used to optimize long-term peripheral T-cell engraftment in these human-mouse chimeras and may also be useful in clinical treatment of T-cell deficiencies.
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Spain, B. A., D. M. Soliman, R. A. Sidner, and H. L. Twigg. "Enhanced proliferation and IL-2 secretion by lung lymphocytes from HIV-infected subjects." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 4 (October 1, 1995): L498—L506. http://dx.doi.org/10.1152/ajplung.1995.269.4.l498.
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Human immunodeficiency virus (HIV)-positive patients frequently develop a CD3+/CD8+ cytotoxic T cell lymphocytic alveolitis. This could occur through in situ expansion of lung lymphocytes. We evaluated lung and blood lymphocyte proliferation in asymptomatic HIV-infected individuals by measuring spontaneous and cytokine-induced tritiated thymidine incorporation. Interleukin (IL)-2 and IL-4 secretion was determined with the use of enzyme-linked immunosorbent assay, Western blotting, and immunoprecipitation techniques. Spontaneous proliferation by lung lymphocytes from HIV-positive patients was significantly greater than that of normal volunteers. Proliferation was confined to the CD8+ lymphocyte subset. Over time, spontaneous proliferation declined unless autologous alveolar macrophages (AM) were added, suggesting AM were providing additional stimulatory signals to lung lymphocytes. Lung and blood lymphocytes proliferated in response to IL-2 but not IL-4. Lymphocytes in HIV-infected lung spontaneously produced and secreted more IL-2 than either normal lung lymphocytes or autologous blood lymphocytes. IL-4 production was not detectable in either group. These findings support the hypothesis that lymphocytic alveolitis in asymptomatic HIV-positive patients results from IL-2-dependent in situ proliferation of CD3+/CD8+ cytotoxic T cells.
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Yang, Yu, Peng-Lei Xiao, Ya Yang, Jian-Chuan Gao, Yan Shi, Wan-Ting Cheng, Yue Chen, Xiu-Xia Song, Qing-Wu Jiang, and Yi-Biao Zhou. "Immune Dysfunction and Coinfection with Human Immunodeficiency Virus and Schistosoma japonicum in Yi People." Journal of Immunology Research 2018 (July 2, 2018): 1–9. http://dx.doi.org/10.1155/2018/6989717.
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Objective. To explore the association between infections with HIV and Schistosoma japonicum, and to determine the influences of the HIV-S. japonicum coinfections on the immune system of Yi people. Methods. A block design study was conducted in a Yi county in southwestern China, one of the endemic areas of both HIV/AIDS and S. japonicum in China. All participants were screened for HIV antibodies and S. japonicum antibodies (SjAb) and were classified into four groups: HIV(+)/S. japonicum(−), HIV(−)/S. japonicum (+), HIV(+)/S. japonicum(+), and HIV(−)/S. japonicum(−). Results. There were significant differences among the four groups in both CD4+ T lymphocytes and CD8+ T lymphocytes, but no significant difference in CD3+ T lymphocytes. Both the CD4+ T lymphocyte counts and the ratio of CD4+/CD8+ were lower in HIV-infected people compared with those uninfected. People infected with S. japonicum had increased CD4+ T lymphocyte counts but reduced CD8+ T lymphocyte counts. Similarly, the ratio of CD4+/CD8+ was higher in S. japonicum-infected people compared with those uninfected. People coinfected with HIV and S. japonicum had lower CD4+ T lymphocyte counts, lower ratio of CD4+/CD8+, and higher CD8+ T lymphocyte counts compared with those infected with HIV only or S. japonicum only. People infected with HIV only and those coinfected with HIV and S. japonicum had a higher level of IFN-γ compared with people with no infection. There were no significant differences between people infected with HIV only and with S. japonicum only in the levels of IFN-γ and IL-10. Conclusions. People coinfected with HIV and S. japonicum might have a suppressed immune function because of a decrease in CD4+ T lymphocyte counts, a lowered ratio of CD4+/CD8+, and an increase in CD8+ T lymphocyte counts. Coinfection with HIV and S. japonicum would alter the level of IFN-γ in plasma.
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Weller, Peter F., and Kaiser Lim. "Human eosinophil-lymphocyte interactions." Memórias do Instituto Oswaldo Cruz 92, suppl 2 (December 1997): 173–82. http://dx.doi.org/10.1590/s0074-02761997000800023.
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Ramesh, Kashi S., Stephanie H. Pincus, and Ross E. Rocklin. "Human lymphocyte-eosinophil interactions." Cellular Immunology 92, no. 2 (May 1985): 366–75. http://dx.doi.org/10.1016/0008-8749(85)90018-8.
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Karlsson, Gunilla B., Matilda Halloran, Dominik Schenten, Juliette Lee, Paul Racz, Klara Tenner-Racz, Judith Manola, et al. "The Envelope Glycoprotein Ectodomains Determine the Efficiency of CD4+ T Lymphocyte Depletion in Simian– Human Immunodeficiency Virus–Infected Macaques." Journal of Experimental Medicine 188, no. 6 (September 21, 1998): 1159–71. http://dx.doi.org/10.1084/jem.188.6.1159.
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CD4+ T lymphocyte depletion in human immunodeficiency virus type 1 (HIV-1)–infected humans underlies the development of acquired immune deficiency syndrome. Using a model in which rhesus macaques were infected with chimeric simian–human immunodeficiency viruses (SHIVs), we show that both the level of viremia and the structure of the HIV-1 envelope glycoprotein ectodomains individually contributed to the efficiency with which CD4+ T lymphocytes were depleted. The envelope glycoproteins of recombinant SHIVs that efficiently caused loss of CD4+ T lymphocytes exhibited increased chemokine receptor binding and membrane-fusing capacity compared with those of less pathogenic viruses. These studies identify the HIV-1 envelope glycoprotein ectodomains as determinants of CD4+ T lymphocyte loss in vivo and provide a foundation for studying pathogenic mechanisms.
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Hatzistilianou, Marija, Soultana Hitoglou, Despina Gougoustamou, Alexandros Kotsis, Athanasios Kallinderes, Fanni Athanassiadou, and Dorothea Catriu. "Effects of immunoregulatory drugs on human peripheral blood T lymphocytes function in vitro." Archive of Oncology 10, no. 1 (2002): 19–23. http://dx.doi.org/10.2298/aoo0201019h.
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BACKGROUND: The purpose of the study was to evaluate the mode of action of different immunoregulatory drugs in lymphocyte proliferation and activation METHODS: The drugs studied were prednisolone (PRED), cyclosporin A (CsA) the recombination of PRED and CsA, L-asparaginase and cytosine-arabinose (ara-C). Peripheral blood lymphocytes from normal blood donors were stimulated by phytohemagglutinin (PHA). Lymphocytes proliferation and activation were determined by tritiated thymidine ([3H]TdR) incorporation secretion of interleukin-2, level of soluble interleukin-2 receptors in the supernatant of the culture medium, and immunophenotyping analysis of T lymphocyte subsets. RESULTS: Among PRED CsA and their combination, the strongest inhibition of cell proliferation was induced by PRED while L-asparaginase and ara-C inhibited PHA stimulated T cells proliferation in concentration and time dependent manner. Among PRED, CsA and their combination, CsA induced the greatest inhibition of IL-2 production. All the immunoregulatory drugs inhibited lymphocyte proliferation and expression of activation antigens. CONCLUSION: The immunoregulatory drugs inhibit both lymphocyte proliferation and activation but in a different way.
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de los Toyos, J., S. Jalkanen, and EC Butcher. "Flow cytometric analysis of the Hermes homing-associated antigen on human lymphocyte subsets." Blood 74, no. 2 (August 1, 1989): 751–60. http://dx.doi.org/10.1182/blood.v74.2.751.751.
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Abstract The homing of lymphocytes is controlled by interactions with high endothelial venules (HEV), specialized vessels that define sites of lymphocyte extravasation into lymph nodes and inflamed tissues. In humans, lymphocyte-HEV binding involves a lymphocyte surface glycoprotein (GP) of 85 to 95 kd (CD44, H-CAM), defined by monoclonal antibody (MoAb) Hermes-1. To define the expression of this homing- associated adhesion molecule during human lymphocyte development, we performed two-color immunofluorescence analyses of human bone marrow (BM), thymus, peripheral blood (PB), and tonsillar lymphocytes. The highest levels of Hermes-1 antigen are displayed by circulating B and T cells in the blood, which are uniformly positive and bear roughly twice the level of antigen present on mature lymphocytes within organized lymphoid tissues and BM. “Immature” (CD4+, CD8+) T cells in the thymus are Hermes-1lo to-, whereas thymocytes of mature phenotype (CD4+ or CD8+) are positive. The Hermes-1 antigen is present at high levels on the same population of thymocytes that bears high surface levels of CD3, a component of the T-cell antigen receptor complex, suggesting that levels of T-cell homing and antigen receptors characteristic of mature peripheral T cells appear coordinately during thymocyte maturation/selection. Essentially all T cells in the periphery are Hermes-1hi, including T blasts, and the homing-associated antigen is maintained at high levels on T cells stimulated in vitro by phytohemagglutinin (PHA) and on interleukin-2 (IL-2) maintained T-cell clones and lines. In contrast, although most resting IgD+ B cells are positive a significant fraction of B cells in tonsils are Hermes-1lo to- ; these cells are predominantly PNAhi, IgD-, and CD20hi, a phenotype characteristic of sessile, activated B cells in germinal centers. In all lymphocyte populations examined, there is a linear correlation in staining for Hermes-1 and for Hermes-3, an antibody that defines a distinct functionally important epitope on this molecule. The results demonstrate a precise regulation of this homing-associated antigen during lymphocyte differentiation.
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de los Toyos, J., S. Jalkanen, and EC Butcher. "Flow cytometric analysis of the Hermes homing-associated antigen on human lymphocyte subsets." Blood 74, no. 2 (August 1, 1989): 751–60. http://dx.doi.org/10.1182/blood.v74.2.751.bloodjournal742751.
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The homing of lymphocytes is controlled by interactions with high endothelial venules (HEV), specialized vessels that define sites of lymphocyte extravasation into lymph nodes and inflamed tissues. In humans, lymphocyte-HEV binding involves a lymphocyte surface glycoprotein (GP) of 85 to 95 kd (CD44, H-CAM), defined by monoclonal antibody (MoAb) Hermes-1. To define the expression of this homing- associated adhesion molecule during human lymphocyte development, we performed two-color immunofluorescence analyses of human bone marrow (BM), thymus, peripheral blood (PB), and tonsillar lymphocytes. The highest levels of Hermes-1 antigen are displayed by circulating B and T cells in the blood, which are uniformly positive and bear roughly twice the level of antigen present on mature lymphocytes within organized lymphoid tissues and BM. “Immature” (CD4+, CD8+) T cells in the thymus are Hermes-1lo to-, whereas thymocytes of mature phenotype (CD4+ or CD8+) are positive. The Hermes-1 antigen is present at high levels on the same population of thymocytes that bears high surface levels of CD3, a component of the T-cell antigen receptor complex, suggesting that levels of T-cell homing and antigen receptors characteristic of mature peripheral T cells appear coordinately during thymocyte maturation/selection. Essentially all T cells in the periphery are Hermes-1hi, including T blasts, and the homing-associated antigen is maintained at high levels on T cells stimulated in vitro by phytohemagglutinin (PHA) and on interleukin-2 (IL-2) maintained T-cell clones and lines. In contrast, although most resting IgD+ B cells are positive a significant fraction of B cells in tonsils are Hermes-1lo to- ; these cells are predominantly PNAhi, IgD-, and CD20hi, a phenotype characteristic of sessile, activated B cells in germinal centers. In all lymphocyte populations examined, there is a linear correlation in staining for Hermes-1 and for Hermes-3, an antibody that defines a distinct functionally important epitope on this molecule. The results demonstrate a precise regulation of this homing-associated antigen during lymphocyte differentiation.
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Stoolman, LM, TA Yednock, and SD Rosen. "Homing receptors on human and rodent lymphocytes--evidence for a conserved carbohydrate-binding specificity." Blood 70, no. 6 (December 1, 1987): 1842–50. http://dx.doi.org/10.1182/blood.v70.6.1842.1842.
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Abstract Lymphocyte recirculation begins with the attachment of circulating cells to the structurally distinctive postcapillary venules of lymphoid organs termed high-endothelial venules (HEVs). In both rodents and humans, the attachment of lymphocytes to the HEVs of peripheral lymph nodes (PNs) on the one hand and gut-associated lymphoid tissues (GALTs) on the other appears to involve discrete adhesive structures on the surfaces of the interacting cells. In rodents, we previously showed that a carbohydrate-binding receptor at the lymphocyte surface participates in the attachment to the HEV of peripheral nodes. The studies reported herein document the involvement of a similar receptor in the selective attachment of human peripheral blood lymphocytes to the HEVs of PNs. We argue that the close functional relationship between the human and rodent receptors indicates that this component of the adhesive interaction has been conserved through evolution.
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Stoolman, LM, TA Yednock, and SD Rosen. "Homing receptors on human and rodent lymphocytes--evidence for a conserved carbohydrate-binding specificity." Blood 70, no. 6 (December 1, 1987): 1842–50. http://dx.doi.org/10.1182/blood.v70.6.1842.bloodjournal7061842.
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Lymphocyte recirculation begins with the attachment of circulating cells to the structurally distinctive postcapillary venules of lymphoid organs termed high-endothelial venules (HEVs). In both rodents and humans, the attachment of lymphocytes to the HEVs of peripheral lymph nodes (PNs) on the one hand and gut-associated lymphoid tissues (GALTs) on the other appears to involve discrete adhesive structures on the surfaces of the interacting cells. In rodents, we previously showed that a carbohydrate-binding receptor at the lymphocyte surface participates in the attachment to the HEV of peripheral nodes. The studies reported herein document the involvement of a similar receptor in the selective attachment of human peripheral blood lymphocytes to the HEVs of PNs. We argue that the close functional relationship between the human and rodent receptors indicates that this component of the adhesive interaction has been conserved through evolution.
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Nichols, Joan E., Jean A. Niles, and Norbert J. Roberts. "Human Lymphocyte Apoptosis after Exposure to Influenza A Virus." Journal of Virology 75, no. 13 (July 1, 2001): 5921–29. http://dx.doi.org/10.1128/jvi.73.13.5921-5929.2001.
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ABSTRACT Infection of humans with influenza A virus (IAV) results in a severe transient leukopenia. The goal of these studies was to analyze possible mechanisms behind this IAV-induced leukopenia with emphasis on the potential induction of apoptosis of lymphocytes by the virus. Analysis of lymphocyte subpopulations after exposure to IAV showed that a portion of CD3+, CD4+, CD8+, and CD19+ lymphocytes became apoptotic (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling positive). The percentage of cells that are infected was shown to be less than the percentage of apoptotic cells, suggesting that direct effects of cell infection by the virus cannot account fully for the high level of cell death. Removal of monocytes-macrophages after IAV exposure reduced the percent of lymphocytes that were apoptotic. Treatment of virus-exposed cultures with anti-tumor necrosis factor alpha did not reduce the percentage of lymphocytes that were apoptotic. In virus-exposed cultures treated with anti-FasL antibody, recombinant soluble human Fas, Ac-DEVD-CHO (caspase-3 inhibitor), or Z-VAD-FMK (general caspase inhibitor), apoptosis and production of the active form of caspase-3 was reduced. The apoptotic cells were Fas-high-density cells while the nonapoptotic cells expressed a low density of Fas. The present studies showed that Fas-FasL signaling plays a major role in the induction of apoptosis in lymphocytes after exposure to IAV. Since the host response to influenza virus commonly results in recovery from the infection, with residual disease uncommon, lymphocyte apoptosis likely represents a part of an overall beneficial immune response but could be a possible mechanism of disease pathogenesis.
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Wiley, J. S., J. R. Chen, G. P. Jamieson, and P. J. Thurlow. "Agonists for endothelial P2 purinoceptors trigger a signalling pathway producing Ca2+ responses in lymphocytes adherent to endothelial cells." Biochemical Journal 311, no. 2 (October 15, 1995): 589–94. http://dx.doi.org/10.1042/bj3110589.
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Recirculation of lymphocytes through the body involves their frequent adhesion to endothelial cells but little is known of the signalling pathways between these two cell types. Lymphocytes from patients with chronic lymphocytic leukaemia were loaded with the Ca(2+)-sensitive indicator, fura 2, and allowed to adhere to either glass or monolayers of human umbilical-vein endothelial cells. Addition of ATP or UTP (1-10 microM) to the superfusate produced a transient rise in cytosolic Ca2+ concentration in the lymphocytes adherent to endothelium (24 of 35 cells). In contrast, ATP or UTP (1-10 microM) had no effect on the cytosolic Ca2+ of lymphocytes attached to glass. As the only lymphocyte receptor for ATP (P2Z class) requires higher ATP concentrations (> 50 microM) for Ca2+ influx and is unresponsive to UTP, the involvement of a lymphocyte P2Z purinoceptor is unlikely. Various agonists including ATP, UTP, 2-methylthioATP, ADP and histamine all stimulated increases in endothelial cytosolic Ca2+ but only ATP and UTP (both agonists for endothelial P2U purinoceptors) triggered Ca2+ transients in adherent lymphocytes. Removal of extracellular Ca2+ did not abolish the ATP-induced rise in cytosolic Ca2+ concentration in lymphocytes adherent to endothelial cells. These findings show that stimulation of endothelial P2U purinoceptors triggers an endothelial-lymphocyte signalling pathway which releases internal Ca2+ in adherent lymphocytes.
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Davodeau, F., M. A. Peyrat, F. Romagné, A. Necker, M. M. Hallet, H. Vié, and M. Bonneville. "Dual T cell receptor beta chain expression on human T lymphocytes." Journal of Experimental Medicine 181, no. 4 (April 1, 1995): 1391–98. http://dx.doi.org/10.1084/jem.181.4.1391.
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Allelic exclusion of lymphocyte antigen receptor chains has been hypothesized as a mechanism developed by the immune system to ensure efficient lymphocyte repertoire selection and tight control of lymphocyte specificity. It was effectively shown to be operative for both the immunoglobulin (Ig) and the T cell receptor (TCR) beta chain genes. Our present observations suggest that close to 1% of human T lymphocytes escape this allelic control, and express two surface TCR beta chains with distinct superantigenic reactivities. Since this high frequency of dual beta chain expressors did not result in any dramatic immune dysregulations, these results question the need for a mechanism ensuring clonal monospecificity through allelic exclusion.
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Tarsis, Sara L., Ming-Tsung Yu, Elizabeth S. Parks, Deborah Persaud, José L. Muñoz, and Wade P. Parks. "Human T-Lymphocyte Transformation with Human T-Cell Lymphotropic Virus Type 2." Journal of Virology 72, no. 1 (January 1, 1998): 841–46. http://dx.doi.org/10.1128/jvi.72.1.841-846.1998.
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ABSTRACT Human T-cell lymphotrophic virus type 2 (HTLV-2), a common infection of intravenous drug users and subpopulations of Native Americans, is uncommon in the general population. In contrast with the closely related HTLV-1, which is associated with both leukemia and neurologic disorders, HTLV-2 lacks a strong etiologic association with disease. HTLV-2 does shares many properties with HTLV-1, including in vitro lymphocyte transformation capability. To better assess the ability of HTLV-2 to transform lymphocytes, a limiting dilution assay was used to generate clonal, transformed lymphocyte lines. As with HTLV-1, the transformation efficiency of HTLV-2 producer cells was proportionately related to the number of lethally irradiated input cells and was comparable to HTLV-1-mediated transformation efficiency. HTLV-2-infected cells were reproducibly isolated and had markedly increased growth potential compared to uninfected cells; HTLV-2 transformants required the continued presence of exogenous interleukin 2 for growth for several months and were maintained for over 2 years in culture. All HTLV-2-transformed populations were CD2 and/or CD3 positive and B1 negative and were either CD4+ or CD8+ populations or a mixture of CD4+ and CD8+ lymphocytes. Clonality of the HTLV-2 transformants was confirmed by Southern blot analysis of T-cell receptor β chain rearrangement. Southern blot analysis revealed a range of integrated full-length genomes from one to multiple. In situ hybridization analysis of HTLV-2 integration revealed no obvious chromosomal integration pattern.
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Thurlow, P. J., L. Kerrigan, R. A. Harris, and I. F. McKenzie. "Analysis of human bone marrow with monoclonal antibodies." Journal of Histochemistry & Cytochemistry 33, no. 12 (December 1985): 1183–89. http://dx.doi.org/10.1177/33.12.2415573.
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In order to study the antigenic phenotype of different hemopoietic cells, we used a series of monoclonal antibodies to investigate normal bone marrow in a standard immunofluorescence assay. The antibodies detected the following antigens: HLA-ABC, beta 2-microglobulin (beta 2m), HLA-DR (Ia), a lymphocyte subset and specific antigen (T and B) HuLy-m2, m3, T lymphocyte antigen (HuLy-m1), lymphocyte T200 antigen (HuLy-m4), a viral-associated antigen (HuLy-m5), and platelet-specific glycoproteins IIb-IIIa (HuPl-m1). The following results were obtained: (a) normoblasts were weakly HLA-ABC+, beta 2m+ and Ia-; all other lymphocyte and platelet antigens were not detected. (b) Myeloid cells at all stages of differentiation (promyelocytes, myelocytes, metamyelocytes, and neutrophils) were HLA-ABC+; beta 2m+; HuLy-m1-, m2-, m3+/- (20%), m4+, m5+/- (20%); HuPl-m1-; in addition, promyelocytes and myelocytes were Ia+ but neutrophils and metamyelocytes were Ia-. (c) Lymphocytes were HLA-ABC+, beta 2m+, Ia+/- (20-30%), HuLy-m1+/- (40-50%), m2+/- (60-70%), m3+, m4+, m5+; Pl-m1-. (d) Platelets and megakaryocytes were HLA-ABC+; beta 2m+; Ia-; HuLy-m1+-, m2-, m3-, m4-, m5-, HuPl-m1+, and the putative "megakaryocyte precursors" were HuPl-m1+, Ia-, HuLy-m1-. The different cell types in bone marrow could readily be distinguished, particularly cells of the myeloid series (Ia and HuLy-m4, m5), lymphocytes (Ia and HuLy-m1, m2, m3), and platelets and their precursor cells (HuPl-m1). This simple method of defining cellular phenotypes in bone marrow has demonstrated the practicality of using monoclonal antibodies to identify marrow cells and should be of diagnostic value.
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Hart, Derek N. J., Min Rao, Xinsheng Ju, and Georgina J. Clark. "Novel Human CD4+ T Lymphocyte Subpopulations Defined by CD300a/c Molecule Expression." Blood 110, no. 11 (November 16, 2007): 2304. http://dx.doi.org/10.1182/blood.v110.11.2304.2304.
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Abstract CD300a and CD300c are leukocyte membrane glycoproteins encoded by genes in the CD300 complex on human chromosome 17. These molecules function as immunoregulatory molecules that initiate triggering and inhibitory responses following ligation with ligands. The CMRF-35 monoclonal antibody binds to an epitope common to both molecules, expressed on most human leukocyte populations, apart from B lymphocytes and a subpopulation of CD4+ and CD8+ T lymphocytes. We used it to study the distribution of the CD300a and CD300c molecules on peripheral blood CD4+ T lymphocytes and defined novel CD300a/c++ , CD300a/c+ and CD300a/c− CD4+ T lymphocyte subpopulations. Resting peripheral CD4+ T lymphocytes express CD300a mRNA and very low amounts of CD300c. Activation results in an initial decrease in CD300a gene expression before an increase in both CD300a and CD300c gene expression. The upregulated expression of these genes was associated with increased CMRF-35 binding to activated T lymphocytes. The CD300a/c− fraction of CD4+ T lymphocytes proliferated to a greater extent than the CD300a/c++ fraction, in response to mitogens or allogeneic antigen. The poor proliferation of the CD300a/c++CD4+ in response to mitogens was explained by increased apoptosis within this subpopulation. The recall antigen, tetanus toxoid, stimulated the CD300a/c++CD4+CD45RO+ but not the CD300a/c−CD4+CD45RO+ subpopulation. Resting CD300a/c++CD4+ lymphocytes express low levels of IFNγ mRNA. Within 18 hours following in vitro activation, CD300a/c++CD4+ lymphocytes express more IFNγ mRNA and protein compared to the CD300a/c−CD4+ lymphocytes, however, after 24 hours both the CD300a/c+ and CD300a/c− CD4+ T lymphocytes were able to produce IFNγ. Th1 and Th17 effector populations are found within the CD300a/c++CD4+ T lymphocyte population, whilst the Treg population are restricted to the CD300a/c−CD4+ T lymphocyte population. Thus, CD300a/c subdivides CD4+ subpopulations into functional populations with the potential to immunoregulate immune and allogeneic responses. We are currently monitoring these populations in allogeneic haemopoietic stem cell recipients.
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Forsyth, Christopher B., and Herbert L. Mathews. "Lymphocyte Adhesion to Candida albicans." Infection and Immunity 70, no. 2 (February 2002): 517–27. http://dx.doi.org/10.1128/iai.70.2.517-527.2002.
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ABSTRACT Adherence of lymphocytes to the fungus is the first step in the direct lymphocyte-mediated antifungal effect against Candida albicans. In this study we identified macrophage-1 antigen (Mac-1) (CD11b/CD18, αM/β2) as the lymphocyte surface structure responsible for the adhesion of activated lymphocytes to the hyphal form of the fungus. Antibodies specific for epitopes of the α-subunit (CD11b) and the β2-subunit (CD18) of Mac-1 were shown to completely eliminate lymphocyte adhesion to C. albicans hyphae. Lymphocyte adhesion to C. albicans was also inhibited significantly by known ligands of Mac-1, including the extracellular matrix proteins laminin and fibrinogen, as well as engineered peptides containing arginine-glycine-aspartic acid sequences and the disintegrin echistatin. N-Acetyl-d-glucosamine and β-glucan, which inhibit Mac-1-mediated adhesion to the yeast, blocked lymphocyte adhesion to hyphae. NIH 3T3 fibroblast transfectants expressing human CD11b/CD18 bound to C. albicans, and their binding was inhibited by antibodies specific for CD11b/CD18. Finally, antibodies specific for CD11b/CD18 effectively inhibited the capacity of activated lymphocytes to have an antifungal effect against hyphae. Our results clearly identify Mac-1 (CD11b/CD18) as the lymphocyte surface structure that mediates activated lymphocyte adhesion to C. albicans and the resultant antifungal effect of the lymphocytes.
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Jiang, Weiming, Laiyi Kang, Hong-Zhou Lu, Xiaozhang Pan, Qingneng Lin, Qichao Pan, Yile Xue, Xinhua Weng, and Yi-Wei Tang. "Normal Values for CD4 and CD8 Lymphocyte Subsets in Healthy Chinese Adults from Shanghai." Clinical Diagnostic Laboratory Immunology 11, no. 4 (July 2004): 811–13. http://dx.doi.org/10.1128/cdli.11.4.811-813.2004.
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ABSTRACT The aim of this study was to establish reference ranges for lymphocyte subsets in Chinese adults. Venous blood specimens were obtained from 614 healthy, human immunodeficiency virus (HIV)-seronegative adults in Shanghai. Flow cytometry was used to determine percentages and absolute numbers of CD4 and CD8 T lymphocytes. Mean values for CD4 and CD8 lymphocytes were 727 and 540 cells/μl, respectively, yielding a CD4/CD8 ratio of 1.49. While CD8 lymphocyte values varied with age and gender, no significant differences in CD4 lymphocyte values were observed. Shanghai adults had approximately 100 fewer CD4 lymphocytes/μl on average than Caucasians, suggesting that lower CD4 lymphocyte cutoffs for classifying and monitoring HIV infection may be needed in China.
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Machado, Heather E., Nina Friesgaard Øbro, Emily Mitchell, Megan Davies, Anthony R. Green, Kourosh Saeb-Parsy, Daniel James Hodson, David Kent, and Peter J. Campbell. "Life History of Normal Human Lymphocytes Revealed By Somatic Mutations." Blood 134, Supplement_1 (November 13, 2019): 1045. http://dx.doi.org/10.1182/blood-2019-128188.
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Introduction: Mature blood cells harbor a mixture of mutations inherited from ancestral hematopoietic stem cells (HSCs) and mutations accumulated after maturation. The landscape of these somatic mutations in normal blood is poorly mapped, with questions as simple as "how many mutations does a memory T cell accumulate throughout life?" remaining unanswered. This gap in our knowledge is particularly relevant for hematopoietic malignancy- while we know that lymphomas derive from lymphocytes of particular stages of differentiation, we do not know if the patterns we see are reflected in their normal counterparts. Results: In order to characterize normal somatic mutation in lymphocytes, we performed single-cell expansion and whole genome sequencing of over 600 T and B lymphocytes and 200 HSC and progenitor cells across 5 individuals (ages 0-85). All lymphocyte subsets show increased mutation burden with respect to HSCs across all classes of variants (Figure 1). Some of this increase can explained by lymphocyte-specific mutational processes, such as the activity of RAG, accounting for at least 20% of observed structural variants. We also find a striking variation in mutation burden within and between lymphocyte subsets. Microenvironment specific mutational processes dominate the observed differences. Examples of this include germinal center ("non-canonical AID") mutations in memory B cells and UV-like mutations in memory T cells (putatively skin resident cells). Naive B and T cells show a lack of variation in discrete mutational patterns relative to their memory counterparts, and have mutational profiles and mutation burdens more similar to that of HSCs. We also observe differences in the mutational patterns between B and T cells that are indicative of the increased divergence of T lymphocytes from the HSC pool. In general, the mutation burden we observe in normal lymphocytes approach those seen in lymphoma. Conclusions: Our work highlights the substantial genetic diversity in normal lymphocytes, with some cells accumulating thousands of mutations on top of those inherited from the HSC compartment. These mutations can be used to describe the life history of each individual lymphocyte including their exposure to specific microenvironments. Our findings shed light on the biology of these cells and will help differentiate between normal and disease processes. Figure 1 Disclosures No relevant conflicts of interest to declare.
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Nishimura, Toshinobu, Shin Kaneko, Haruo Gotoh, Naoya Takayama, Takafumi Shimizu, Shoichi Iriguchi, Yoko Tajima, et al. "Generation of Monoclonal TCR-Expressing Human T-Lineage Lymphocytes From Induced Pluripotent Stem Cells of Single Peripheral T-Lymphocyte Origin." Blood 116, no. 21 (November 19, 2010): 490. http://dx.doi.org/10.1182/blood.v116.21.490.490.
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Abstract Abstract 490 T lymphocytes play central roles in cellular immunity, exerting their proliferative and effector activities when they recognize antigens, in HLA-restricted and antigen-specific manner, via T-cell receptors (TCRs). Successful treatment of leukemias/cancers with T-lymphocytes infusions is a direct proof that human immunity has the potential to eradicate cancers. However, continuous exposure to tumor/self antigens drives T lymphocytes into a highly exhausted state, with loss of potentials for long-term survival, proliferation, and effector functions that can end up with deletion of antigen-responding T-lymphocyte pools. Several workers have endeavored to develop clinical protocols for expanding antigen-responding T cells from the few naïve T-cell pools remaining in the patient. However, highly expanded T cells in such protocols have not proved fully effective so far, because functional losses like those in the patient occur during ex vivo manipulation. To overcome this obstacle to T-lymphocyte based immunotherapy, we endeavored to induce antigen-specific TCR-expressing T lymphocytes from induced pluripotent stem (iPS) cells, which were derived from antigen-reactive single T lymphocytes. iPS cells have a capacity for unlimited self-renewal while maintaining pluripotency. These features enabled us to induce an unlimited number of T lymphocytes, especially naïve T lymphocytes, showing reactivity to specific antigens. If they retain properties of naïve T lymphocytes, they may proliferate for a longer period and achieve better therapeutic effects than their peripheral blood counterparts expanded in vitro. Peripheral T lymphocytes were isolated from healthy volunteers. Then three reprogramming factors (OCT4, SOX2, and KLF4) and additional factors (c-MYC and/or NANOG) were transduced into fresh or frozen/thawed T lymphocytes using a retrovirus. The virus-infected T lymphocytes were then transferred onto mouse embryonic fibroblasts (MEFs) in the presence of cytokines and chemicals favorable for T-lymphocyte survival/proliferation. iPS-like colonies were observed within 3 weeks after infections. Single T lymphocyte-derived colonies were isolated and clonally expanded. They exhibited standard ES-like morphology, cell surface markers and alkaline phosphatase activity, as well as differentiation potential into various tissues related to all three germ layers. Human TCRs are encoded in four genes (TCRA, TCRB, TCRG, TCRD), which should be genetically assembled in an irreversible manner during T-lymphocyte development. This feature allowed us to retrospectively confirm the iPS cells were generated from T lymphocyte. The TCR genes rearrangement encoded in an iPS colony was single in all iPS lines, indicating that the iPS colony was derived from single T lymphocyte. Sequence analyses of TCR genes revealed whether the rearrangements were productive, and the productivity might promise the conservation of TCR genes rearrangement during the reprogramming process. Next, we tried to re-differentiate T-lymphocyte derived-iPS (T-iPS) cells into T-lineage cells by co-culturing them with murine stromal cell layers (OP9 and OP9-DL1). These T-lineage committed cells were expressed TCRab heterodimer and T-cell surface markers such as CD3. They could activate via TCR stimulation, and produce IL-2 and IFN-g as maturing T lymphocytes. The re-differentiation efficiency of T-iPS cells was higher than those of embryonic stem cells, fibroblasts derived-iPS cells, or cord blood derived-iPS cells. mRNA sequence of TCRs transcribed in re-differentiated T-lineage cells was identical to that engraved in the pre-differentiated T-iPS cells genome. The invariance of the sequence, especially antigen-recognition site sequence, indicated that the antigen-specificity in original T lymphocyte was conserved during re-differentiation process. Here we show that the conservation of the antigen-specificity encoded in TCR genes throughout induction of T-iPS cells and re-differentiation into T-lineage cells. These data suggest that further optimization of these processes for clinical application could open the door to the development of novel T-lymphocyte therapy, repeatedly supplying patient-compatible and disease-specific naïve T lymphocytes. Disclosures: No relevant conflicts of interest to declare.
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Berg, E. L., M. K. Robinson, R. A. Warnock, and E. C. Butcher. "The human peripheral lymph node vascular addressin is a ligand for LECAM-1, the peripheral lymph node homing receptor." Journal of Cell Biology 114, no. 2 (July 15, 1991): 343–49. http://dx.doi.org/10.1083/jcb.114.2.343.
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The trafficking of lymphocytes from the blood and into lymphoid organs is controlled by tissue-selective lymphocyte interactions with specialized endothelial cells lining post capillary venules, in particular the high endothelial venules (HEV) found in lymphoid tissues and sites of chronic inflammation. Lymphocyte interactions with HEV are mediated in part by lymphocyte homing receptors and tissue-specific HEV determinants, the vascular addressins. A peripheral lymph node addressin (PNAd) has been detected immunohistologically in mouse and man by monoclonal antibody MECA-79, which inhibits lymphocyte homing to lymph nodes and lymphocyte binding to lymph node and tonsillar HEV. The human MECA-79 antigen, PNAd, is molecularly distinct from the 65-kD mucosal vascular addressin. The most abundant iodinated species by SDS-PAGE is 105 kD. When affinity isolated and immobilized on glass slides, MECA-79 immunoisolated material binds human and mouse lymphocytes avidly in a calcium dependent manner. Binding is blocked by mAb MECA-79, by antibodies against mouse or human LECAM-1 (the peripheral lymph node homing receptor, the MEL-14 antigen, LAM-1), and by treatment of PNAd with neuraminidase. Expression of LECAM-1 cDNA confers PNAd binding ability on a transfected B cell line. We conclude that LECAM-1 mediates lymphocyte binding to PNAd, an interaction that involves the lectin activity of LECAM-1 and carbohydrate determinants on the addressin.
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Kohno, H., and T. Kanno. "Properties and activities of aminopeptidases in normal and mitogen-stimulated human lymphocytes." Biochemical Journal 226, no. 1 (February 15, 1985): 59–65. http://dx.doi.org/10.1042/bj2260059.
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Human peripheral lymphocytes were found to contain at least two distinct aminopeptidases, designated cytosol aminopeptidase and microsomal aminopeptidase, which differed from one another with respect to intracellular localization, substrate specificity, metal-ion activation, Km value and electrophoretic mobility. No change in these aminopeptidase activities was observed in cultured lymphocytes in the absence of mitogen throughout the cultivation period. The addition of phytohaemagglutinin or concanavalin A to the culture medium caused, in dose-dependent manner, a significant increase in cytosol aminopeptidase activity in lymphocytes. On the other hand, no increase in microsomal aminopeptidase activity was observed under the same conditions. The biochemical properties of aminopeptidases in stimulated cultured lymphocytes were identical with those of the enzymes in peripheral lymphocytes and unstimulated cultured lymphocyte. The phytohaemagglutinin dose-response curves for lymphocyte activation as measured by the DNA synthesis rate and for cytosol aminopeptidase activity were observed to be similar. However, when DNA synthesis was temporarily blocked by hydroxyurea, the rate of increase of aminopeptidase activity was unaffected. Pokeweed mitogen only slightly increased the cytosol aminopeptidase activity in cultured lymphocytes, although the lymphocytes were highly activated.
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Dohi, Keiichiro, William J. Kraemer, and Andrea M. Mastro. "Exercise increases prolactin-receptor expression on human lymphocytes." Journal of Applied Physiology 94, no. 2 (February 1, 2003): 518–24. http://dx.doi.org/10.1152/japplphysiol.00004.2002.
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Plasma prolactin has been shown to increase during stress; the immune system is responsive to prolactin and affected by stress. Therefore, this study was undertaken to investigate the effects of acute graded, maximal treadmill exercise on prolactin-receptor expression by lymphocytes. Eight healthy men underwent one exercise and one nonexercise session. Blood was sampled immediately before and after the exercise. On the day of the nonexercise session, two resting blood samples were obtained at the same times as the exercise session samples to act as baseline data. Plasma prolactin concentrations were significantly elevated in response to exercise and correlated positively with total prolactin-receptor expression per B lymphocyte. An increase in total prolactin-receptor expression per B lymphocyte in response to exercise also was observed. In addition, exercise significantly increased the total number of circulating B lymphocytes expressing prolactin receptor as well as the total number of circulating B lymphocytes. These data support the idea that exercise may enhance the interaction between immune target cells and prolactin, a stress hormone capable of enhancing immune function.
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Fairley, Christopher K., Denis Spelman, Alison Street, Ian D. Jennens, W. John Spicer, and Suzanne Crowe. "CD4 Lymphocyte Numbers after Splenectomy in Patients Infected with the Human Immunodeficiency virus." International Journal of STD & AIDS 5, no. 3 (May 1994): 177–81. http://dx.doi.org/10.1177/095646249400500304.
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Splenectomy has been reported to alter inconsistently the CD4 lymphocyte numbers in patients infected with the human immunodeficiency virus (HIV). To further assess the effect of splenectomy we have retrospectively examined the charts of 10 patients who were infected with HIV and who had undergone splenectomy. There was a significant increase in the mean CD4 numbers following splenectomy (mean increase of 326/μl, or 2.1-fold, P = 0.0009), the total lymphocyte numbers (mean increase of 1.55/ml, or 2.2-fold, P = 0.001) and in the CD8 lymphocyte count (mean increase of 968/μl, or 2.3–fold, P = 0.014). No significant difference was observed in the percentage CD4 lymphocytes ( P = 0.95) or in the CD4:CD8 lymphocyte ratio ( P = 0.76). In two patients, symptoms suggestive of impaired immune function developed post-splenectomy, at a time when their CD4 lymphocyte numbers were markedly higher than their pre-splenectomy values. One developed oral candidiasis (CD4 960/μl, percentage CD4 32%), and in one patient a 7 kg weight loss was associated with recurrent mouth ulcers (CD4 680/μl, percentage CD4 7%). We conclude that the total CD4 count increases significantly after splenectomy while the percentage CD4 lymphocyte count and CD4:CD8 lymphocyte ratio do not. Our data suggest that the CD4 lymphocyte count overestimates the immune function in these patients, although our findings are not conclusive.
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Mun, Yeung-Chul, Kyoung-Eun Lee, Jung Mi Kwon, Seung-Hyun Nam, Eun Sun Yoo, Yun-Kyung Bae, Seung-Eun Lee, et al. "Establishment of Effective B Lymphocyte Ex Vivo Expansion on Human Cord Blood Using TPO, SCF, FL, IL-4, IL-10, and CD40L." Blood 104, no. 11 (November 16, 2004): 2882. http://dx.doi.org/10.1182/blood.v104.11.2882.2882.
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Abstract In respect to B lymphocyte-mediated immunity, characteristics of human cord blood are low counts of mature B lymphocytes, deficient expression of CD40L and cytokine production in CD4+ T lymphocytes, defect in the isotype switch of immunoglobulin and the activation of B lymphocytes, and low IgG production of B lymphocytes. These characteristics of the B lymphocyte from human cord blood lead to a delayed B lymphocyte-mediated immune reconstitution and an increased susceptibility to infections after a cord blood transplantation. The mechanism of immunological recostitution after cord blood transplantation has been examined from a variety of viewpoints in experimental models as well as clinical studies. However, problems of sustained immunodeficiency after cord blood transplantation remain to be resolved. The aim of the present study is to establish culture conditions that support the effective B lymphocyte expansion of human cord blood using IL-4, IL-10, and CD40L, to which cytokines are defected in B lymphocyte of human cord blood, and established conditions are compared to previously established cytokine combinations, TPO+SCF+FL in our Lab (Br J Haematol 107:176–185, 1999 & Stem Cells 21:228–235, 2003). To elucidate the effective B lymphocyte-mediated immune reconstitution of cord blood after ex vivo expansion, mononuclear cells, separated from density gradient of Ficoll system, and CD34+ purified cells, isolated from immunomicrobead(MiniMACS) system, were cultured with various combinations of cytokines (TPO+FL+SCF and/or IL-4, IL-10 and CD40L) for 2 weeks or 4 weeks. This then allowed for cytometric analysis after immunofluorescence stain with CD34, CD38 (for HSC analysis) and CD19, IgG and IgM (for B lymphocyte-mediated immune reconstitution) and CD4 (for T helper cell) and CD25 (for lymphocyte activation assay) to be performed. In the B lymphocyte expansion aspect, the immunoglobulin expression, and functional activity, expansion with the TPO+FL+SCF+IL-4+IL-10 combination showed best results in the expression of CD19, CD25, IgG, and IgM. However, the addition of CD40L to those culture condition did not increase expression of CD19, CD25, IgG, and IgM after the expansion of human cord blood. Expansion of CD34+ purified cells was superior to MNCs in the expression of CD19, CD25, IgG, and IgM. In consideration for the duration of cultures, the 2 week culture was superior to the 4 week culture with respect to graft stemness (CD34+CD38- fraction). Our data suggests most superior results were observed from the ex vivo expansion of CD34+ purified cells cultured for 2 weeks with TPO+FL+SCF+IL-4+IL-10, in the B lymphocyte-mediated immune reconstitution and graft stemness aspect. The results of this study warrant further investigation on effective B lymphocyte-mediated immune reconstitution after cord blood transplantation in vivo using ex vivo expanded cord blood.
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Ryu, Hoon, Chang Duk Jun, Bok Soo Lee, Byung Min Choi, Hyung Min Kim, and Hun-Taeg Chung. "Effect of Qigong Training on Proportions of T Lymphocyte Subsets in Human Peripheral Blood." American Journal of Chinese Medicine 23, no. 01 (January 1995): 27–36. http://dx.doi.org/10.1142/s0192415x95000055.
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The effect of Qigong training on proportions of T lymphocyte subsets was investigated in human peripheral blood. We observed that the ratio of CD4+/CD8+ T lymphocytes was increased as much as 50% in a trainee group who practiced Qigong training more than 5 months compared to a normal healthy group who did not practice. The absolute number of CD4+ T lymphocytes was also elevated in trainee group with 100 cells/mm 3 more than in normal healthy group. The positive correlation between the ratio of CD4+/CD8+ T lymphocytes and the ratio of CD4+45RA-/CD4+ CD45RA+ T lymphocytes was shown in the trainee group. In contrast, there was a negative correlation between the ratio of CD4+/CD8+ T lymphocytes and the ratio of CD8+CD57+/CD8+CD57- T lymphocytes in the trainee group. The data indicate that Qigong training affects the profile of lymphocyte subsets in human peripheral blood, especially the proportion of CD4+ T lymphocytes.
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Majstoravich, Sonja, Jinyi Zhang, Susan Nicholson-Dykstra, Stefan Linder, Wilhelm Friedrich, Katherine A. Siminovitch, and Henry N. Higgs. "Lymphocyte microvilli are dynamic, actin-dependent structures that do not require Wiskott-Aldrich syndrome protein (WASp) for their morphology." Blood 104, no. 5 (September 1, 2004): 1396–403. http://dx.doi.org/10.1182/blood-2004-02-0437.
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Abstract Short microvilli cover the surfaces of circulating mammalian lymphocytes. The surfaces of monocytes and neutrophils are very different, containing ruffles as their predominant structure. In this study, we present the first quantitative characterization of lymphocyte microvilli. From analysis of scanning electron micrographs, we find that median microvillar length and surface density range from 0.3 to 0.4 μm and 2 to 4 microvilli/μm2, respectively, on lymphocytes from a variety of sources. As with similar structures from other cells, lymphocyte microvilli contain parallel bundles of actin filaments. Lymphocyte microvilli rapidly disassemble when exposed to the actin-sequestering molecule, Latrunculin A. This disassembly parallels cellular actin filament depolymerization and is complete within 2 minutes, suggesting that lymphocyte microvilli undergo continuous assembly and disassembly. In contrast to previous reports suggesting lymphocyte microvillar density to be reduced on lymphocytes from Wiskott-Aldrich syndrome (WAS) patient, we find no such deficiency in either mouse or human WAS protein (WASp)–deficient lymphocytes. These results suggest that WASp is either not involved in or is redundant in the rapid dynamics of lymphocyte microvilli.
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Schwarz, H., FJ Blanco, J. von Kempis, J. Valbracht, and M. Lotz. "ILA, a member of the human nerve growth factor/tumor necrosis factor receptor family, regulates T-lymphocyte proliferation and survival." Blood 87, no. 7 (April 1, 1996): 2839–45. http://dx.doi.org/10.1182/blood.v87.7.2839.bloodjournal8772839.
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ILA, a gene induced by lymphocyte activation, is a member of the human nerve growth factor tumor necrosis factor receptor family and the human homologue of murine 4–1BB. The present study analyzed the role of ILA in the regulation of human peripheral blood T-lymphocyte function. Antibodies raised against different fusion proteins recognized ILA on activated lymphocytes. These antibodies significantly increased anti- CD3--induced T-lymphocyte proliferation. When anti-CD3--stimulated cells were incubated on ILA-expressing CHO cells, proliferation was inhibited. CHO cells transfected with a control construct and not expressing ILA did not reduce T-cell proliferation. A purified fusion protein containing the extracellular domain of ILA and the constant domain of human IgG (ILA-IgG) also inhibited lymphocyte proliferation. Results obtained by 3H-thymidine incorporation were confirmed by cell cycle analysis that showed a decrease in the number of lymphocytes in S phase. Lymphocyte morphology in cultures with ILA-expressing CHO cells was suggestive of apoptosis. Flow cytometry on propidium iodide-stained cells showed a time-dependent increase in the number of hypodiploid apoptotic cells when lymphocytes were cultured on ILA-expressing CHO cells. Internucleosomal DNA cleavage was seen in these cultures, but not in the presence of ILA-negative CHO cells. Studies on the mechanism by which ILA regulates T-cell function showed that ILA-IgG inhibited anti-CD3-induced T-cell proliferation when presented in immobilized but not in soluble form. These results suggest that ILA may act by cross- linking its ligand and thereby inhibit T-cell proliferation.
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Kwack, Kyu Hwan, and Hyeon-Woo Lee. "Progranulin Inhibits Human T Lymphocyte Proliferation by Inducing the Formation of Regulatory T Lymphocytes." Mediators of Inflammation 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/7682083.
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We have examined the effect of progranulin (PGRN) on human T cell proliferation and its underlying mechanism. We show that PGRN inhibits the PHA-induced multiplication of T lymphocytes. It increases the number of iTregs when T lymphocytes are activated by PHA but does not do so in the absence of PHA. PGRN-mediated inhibition of T lymphocyte proliferation, as well as the induction of iTregs, was completely reversed by a TGF-β inhibitor or a Treg inhibitor. PGRN induced TGF-β secretion in the presence of PHA whereas it did not in the absence of PHA. Our findings indicate that PGRN suppresses T lymphocyte proliferation by enhancing the formation of iTregs from activated T lymphocytes in response to TGF-β.
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Pfau, S., D. Leitenberg, H. Rinder, B. R. Smith, R. Pardi, and J. R. Bender. "Lymphocyte adhesion-dependent calcium signaling in human endothelial cells." Journal of Cell Biology 128, no. 5 (March 1, 1995): 969–78. http://dx.doi.org/10.1083/jcb.128.5.969.
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Vascular endothelial cells (ECs) can undergo dramatic phenotypic and functional alterations in response to humoral and cellular stimuli. These changes promote endothelial participation in the inflammatory response through active recruitment of immune effector cells, increased vascular permeability, and alteration in vascular tone. In an attempt to define early events in lymphocyte-mediated EC signaling, we investigated cytosolic-free calcium (Ca2+) changes in single, Fluo-3-labeled human umbilical vein ECs (HUVECs), using an ACAS interactive laser cytometer. Of all lymphocyte subsets tested, allogeneic CD3-, CD56+ natural killer (NK) cells uniquely elicited oscillatory EC Ca2+ signals in cytokine (interleukin [IL]-1- or tumor necrosis factor [TNF])-treated ECs. The induction of these signals required avid intercellular adhesion, consisted of both Ca2+ mobilization and extracellular influx, and was associated with EC inositol phosphate (IP) generation. Simultaneous recording of NK and EC Ca2+ signals using two-color fluorescence detection revealed that, upon adhesion, NK cells flux prior to EC. Lymphocyte Ca2+ buffering with 1,2-bis-5-methyl-amino-phenoxylethane-N,N,N'-tetra-acetoxymethyl acetate (MAPTAM) demonstrated that lymphocyte fluxes are, in fact, prerequisites for the adhesion-dependent EC signals. mAb studies indicate that the beta 2 integrin-intercellular adhesion molecule (ICAM)-1 adhesion pathway is critically involved. However, ICAM-1 antisense oligonucleotide inhibition of IL-1-mediated ICAM-1 hyperinduction had no effect on EC Ca2+ signaling in lymphocyte-EC conjugates, indicating that additional cytokine-induced EC alteration is required. These experiments combine features of lymphocyte-endothelial interactions, intercellular adhesion, EC cytokine activation and transmembrane signaling. The results implicate the IP/Ca2+ second messenger pathway in EC outside-in signaling induced by cytotoxic lymphocytes, and suggest that these signals may play a role in EC alteration by lymphocyte adhesion.
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Joksić, Gordana, Sandra Petrović, Ivana Joksić, and Andreja Leskovac. "Biological Effects of Echinacea Purpurea on Human Blood Cells." Archives of Industrial Hygiene and Toxicology 60, no. 2 (June 1, 2009): 165–72. http://dx.doi.org/10.2478/10004-1254-60-2009-1920.
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Biological Effects of Echinacea Purpurea on Human Blood CellsThe aim of this study was to investigate radioprotective properties of Echinacea purpurea tablets in vivo. We analysed lymphocyte chromosome aberrations (CA), micronuclei (MN), apoptosis of leukocytes and haematological parameters in a group of radiation workers who were identified as carrying dicentric chromosomes in their lymphocytes. All radiation workers were taking two 275 mg Echinacea tablets b.i.d., according to a pharmacist's recommendation. All parameters were analysed before and after the two-week treatment. At the end of the treatment lymphocyte CA frequency dropped significantly, and the number of apoptotic cells increased. The inverse lymphocyte-to-granulocyte ratio at the beginning of the study changed to normal at its end. In conclusion, biological effects observed after administration of Echinacea purpurea preparation suggest that it may be beneficial for the prevention of adverse health effects in workers exposed to ionising radiation.
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McKay, Paul F., Dan H. Barouch, Jörn E. Schmitz, Ronald S. Veazey, Darci A. Gorgone, Michelle A. Lifton, Kenneth C. Williams, and Norman L. Letvin. "Global Dysfunction of CD4 T-Lymphocyte Cytokine Expression in Simian-Human Immunodeficiency Virus/SIV-Infected Monkeys Is Prevented by Vaccination." Journal of Virology 77, no. 8 (April 15, 2003): 4695–702. http://dx.doi.org/10.1128/jvi.77.8.4695-4702.2003.
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ABSTRACT Human immunodeficiency virus type 1 infection results in a dysfunction of CD4+ T lymphocytes. The intracellular events contributing to that CD4+ T-lymphocyte dysfunction remain incompletely elucidated, and it is unclear whether aspects of that dysfunction can be prevented. The present studies were pursued in a rhesus monkey model of AIDS to explore these issues. Loss of the capacity of peripheral blood CD4+ T lymphocytes to express cytokines was first detected in simian immunodeficiency virus-infected monkeys during the peak of viral replication during primary infection and persisted thereafter. Moreover, infected monkeys with progressive disease had peripheral blood CD4+ T lymphocytes that expressed significantly less cytokine than infected monkeys that had undetectable viral loads and intact CD4+ T-lymphocyte counts. Importantly, CD4+ T lymphocytes from vaccinated monkeys that effectively controlled the replication of a highly pathogenic immunodeficiency virus isolate following a challenge had a preserved functional capacity. These observations suggest that an intact cytokine expression capacity of CD4+ T lymphocytes is associated with stable clinical status and that effective vaccines can mitigate against CD4+ T-lymphocyte dysfunction following an AIDS virus infection.
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Loffredo, John T., Eva G. Rakasz, Juan Pablo Giraldo, Sean P. Spencer, Kelly K. Grafton, Sarah R. Martin, Gnankang Napoé, Levi J. Yant, Nancy A. Wilson, and David I. Watkins. "Tat28-35SL8-Specific CD8+ T Lymphocytes Are More Effective than Gag181-189CM9-Specific CD8+ T Lymphocytes at Suppressing Simian Immunodeficiency Virus Replication in a Functional In Vitro Assay." Journal of Virology 79, no. 23 (December 15, 2005): 14986–91. http://dx.doi.org/10.1128/jvi.79.23.14986-14991.2005.
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ABSTRACT Epitope-specific CD8+ T lymphocytes may play an important role in controlling human immunodeficiency virus (HIV)/simian immunodeficiency virus replication. Unfortunately, standard cellular assays do not measure the antiviral efficacy (the ability to suppress virus replication) of CD8+ T lymphocytes. Certain epitope-specific CD8+ T lymphocytes may be better than others at suppressing viral replication. We compared the antiviral efficacy of two immunodominant CD8+ T lymphocyte responses—Tat28-35SL8 and Gag181-189CM9—by using a functional in vitro assay. Viral suppression by Tat-specific CD8+ T lymphocytes was consistently greater than that of Gag-specific CD8+ T lymphocytes. Such differences in antigen-specific CD8+-T-lymphocyte efficacy may be important for selecting CD8+ T lymphocyte epitopes for inclusion in future HIV vaccines.
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Dorward, D. "Interactions Between Mouse Lymphocytes And Borrelia Burgdorferi, The Infectious Agent Of Lyme Disease." Microscopy and Microanalysis 5, S2 (August 1999): 1242–43. http://dx.doi.org/10.1017/s143192760001953x.
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Lyme disease is a tick borne, multi-system disorder caused by low density systemic infections with the spirochete Borrelia burgdorferi. Without antimicrobial treatment, mammalian infections with these bacteria are persistent and chronic. Recent studies showed that B. burgdorferi can target, invade, and lyse both cultured and primary human B and T cells. Direct interactions between the spirochetes and lymphocytes also leads to adherence of B and T cell antigens on the surface of significant proportions of the bacteria . Adherent lymphocytic antigens inhibit binding of antibodies to prominent B. burgdorferi proteins, and interfere with classic complement-mediated killing, suggesting a possible role for spirochete-lymphocyte interactions in immune evasion.In order to develop an experimental animal model for assessing spirochete-lymphocyte interactions, B. burgdorferi and primary mouse lymphocytes were co-incubated and examined by electron microscopy. Mononuclear cells were separated from fresh mouse blood by Ficoll gradient centrifugation (ICN, Biomedicals, Aurora, Ohio).
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Tedder, T. F., C. M. Isaacs, T. J. Ernst, G. D. Demetri, D. A. Adler, and C. M. Disteche. "Isolation and chromosomal localization of cDNAs encoding a novel human lymphocyte cell surface molecule, LAM-1. Homology with the mouse lymphocyte homing receptor and other human adhesion proteins." Journal of Experimental Medicine 170, no. 1 (July 1, 1989): 123–33. http://dx.doi.org/10.1084/jem.170.1.123.
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A cDNA encoding a new human lymphocyte cell surface molecule has been isolated and shown to identify a fourth member of a recently discovered family of adhesion proteins. This lymphocyte-associated molecule (LAM-1) is uniquely composed of multiple distinct domains, one domain homologous with animal lectins, one homologous with epidermal growth factor, and two short consensus repeat units similar to those found in C3/C4 binding proteins. This cDNA clone hybridized with RNAs found in B cell lines and T lymphocytes, but not with RNA from other cell types. The amino acid sequence of LAM-1 is 77% homologous with the sequence of the mouse lymphocyte homing receptor, suggesting that LAM-1 may function in human lymphocyte adhesion. The LAM-1 gene is located on chromosome 1q23-25, as is another member of this adhesion family, suggesting that this new family of proteins may be encoded by a cluster of "adhesion protein" loci.
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Boyer, Cinda M., Donna D. Kostyu, Cynthia S. Brissette, and D. Bernard Amos. "Functional defect of heat-inactivated human lymphocytes in mixed-lymphocyte culture." Cellular Immunology 101, no. 2 (September 1986): 440–53. http://dx.doi.org/10.1016/0008-8749(86)90156-5.
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Plum, J., P. Van Cauwenberge, and Magda De Smedt. "Human tonsillar T lymphocytes: An immature or activated T-lymphocyte population." Clinical Immunology and Immunopathology 39, no. 1 (April 1986): 14–23. http://dx.doi.org/10.1016/0090-1229(86)90201-1.
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Kuta, A. E., and L. L. Baum. "C-reactive protein is produced by a small number of normal human peripheral blood lymphocytes." Journal of Experimental Medicine 164, no. 1 (July 1, 1986): 321–26. http://dx.doi.org/10.1084/jem.164.1.321.
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Biosynthetic labeling with [35S]met and immunoprecipitation with anti-C-reactive protein (CRP) antibodies and Staphylococcus aureus indicate that cell surface CRP is produced by lymphocytes. The ability of anti-CRP to reduce NK activity, and the demonstration that 125I-anti-CRP-labeled PBL are found in low-density Percoll fractions associated with large granular lymphocyte (LGL) and NK activity suggest that S-CRP-bearing cells are NK effectors. The production of S-CRP by LGL supports this hypothesis. While lymphocytes were shown to synthesize S-CRP, monocytes produced no detectable S-CRP. The lymphocytes that produce S-CRP apparently do not secrete it; when lymphocyte culture supernatants were tested, no S-CRP was found. This is the first description of extrahepatic synthesis of CRP.
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Hickling, Julian K. "Measuring human T-lymphocyte function." Expert Reviews in Molecular Medicine 1, no. 6 (October 13, 1998): 1–20. http://dx.doi.org/10.1017/s1462399498000313.
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T lymphocytes (T cells) play critical roles in the regulation of immune responses, and are responsible for mediating many of the effector mechanisms of the immune system. For this reason, there has always been a need for assays to measure accurately the activity of populations of T cells, both in model (animal) systems and in humans. The expansion of the biotechnology industry has led to a dramatic increase in the number of novel immunotherapeutics that are being developed for the treatment of cancer, autoimmune disorders and infectious diseases. This increase in activity in the field of immunotherapy, coupled with the expense of clinical trials, has led to renewed interest in methods that accurately assess T-cell function, as researchers seek to maximise the amount of information that can be obtained from each clinical study. Assessing the quantitative and qualitative nature of a T-cell response, for example following vaccination or immunosuppressive therapy, can provide valuable information about the efficacy of a treatment, in place of a clinical endpoint. This article reviews some of the established methods that are used to monitor human T-cell activity, and describes some new approaches that are in development to increase the speed, sensitivity and relevance of such methods.
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De Bartolo, Loredana, Antonella Piscioneri, Sabrina Morelli, Giuseppina Cotroneo, Franco Tasselli, Maria Cristina Caroleo, and Enrico Drioli. "Human lymphocyte hollow fiber bioreactor." Desalination 199, no. 1-3 (November 2006): 141–43. http://dx.doi.org/10.1016/j.desal.2006.03.031.
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Boyd, Scott D., Yi Liu, Chen Wang, Victoria Martin, and Deborah K. Dunn-Walters. "Human lymphocyte repertoires in ageing." Current Opinion in Immunology 25, no. 4 (August 2013): 511–15. http://dx.doi.org/10.1016/j.coi.2013.07.007.
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